It is a sunny January afternoon at the ER when you are called to see a 57 year old male complaining of feeling "really sick".

You find your patient lying in the bed in room 3. He looks pale and short of breath. You introduce yourself and ask him why he has come in today.

He says:

"About two weeks ago, I started feeling short of breath, with a cough. I got much more tired than usual. I went to see my doctor, who said I had an upper respiratory infection and prescribed me some antibiotics. I rested at home for a few days, and started to feel a little better. Then, I began to go downhill again. Felt so awful today, barely have enough energy to walk, so I had my wife drive me to the ER."

He tells you that he has a history of hypertension and is a pack a day smoker, although he is trying to quit., Prior to getting sick, he has felt pretty well. In fact, he tells you that he started a work out regiment to lose some of the excess weight he is carrying.

Your patient tells you he hasn't been eating or drinking well lately, and he is hypotensive at 86/58.

As you are running through your list of differentials, the tech hands you this 12 lead ECG:

You take a look at the ECG, and a couple of thoughts come to mind. You have an idea of what might have happened.

You tell Mr. Wilson that you want to run a few tests…

So, what do you think is wrong with Mr. Wilson?

18 Comments

This gentleman can have an anteroseptal infarction (ST concordance in V1-V3). RBBB pattern should have disconcordant ST depressions in V1-V3…
So I think it´s – Bifascicular block + Anteroseptal STEMI..

Negative component of P can be seen in V1 – LAE
QRS is wide, indicating RBBB. Loss of septal r wave in V1-V3. Poor R wave progression in precordial leads and low voltage.
S wave > R wave in inferior leads + LAD – LAHB
So this is a bifascicular block – RBBB + LAHB
There are upright Ts in V2-V3 with the ST segment being isoelectric instead of the typical strain pattern seen in lead I and avL
I believe this is early presentation of anterior STEMI with bifascicular block. The point that it has persisted for several days meaning that this is probably is a subacute STEMI.

ECG revealed complete RBBB with Rt axis deviation, high normal PR interval and negative P in V1. So, it could be bifascicular block suggestive of early anterior wall myocardial infarction. However, it may be more likely to be pulmonary embolism if no RBBB in previous ECGs

RBBB patten with inappropriate concordance of ST segment best seen in v2 & v3. pathological q waves also noted in acroos right praecordial leads. ST segment depression seen in the inferior leads, and lead I, avL, v5 & 6. Other features noted are STE in avR, LAD most likely due to LAFB (bifascicular block). The first thing that worries me in Mr Wilson is subacute anteroseptal MI with high LAD artery occlusion with widespread subendocardial ischemia.

Rhythm: Regular, p-waves present, P:QRS 1:1, I think PRi is <=0.20s (looking at III group #2 where the p-wave starts at the line, the R-wave starts right before slight before the line, V2, where the p-wave starts in group #9, the q-wave starts before the line), QRS is wide (almost 0.20 itself). Normal sinus rhythm (NSR).

Enlargement: P-wave in II is probably about 2-2.5 mm height, second half of the p-wave in V1 is deep and wide, left atrial enlargement (LAE).

ST/T, Q: Significant q-waves in V1-V4. Anteroseptal infarct of unknown age. Unsure if my eyes are playing tricks with me, looks like slight ST depression in lead I. Inappropriate T-waves for BBB in I, aVR, V1-V4.

I both hate and love getting tough ones, lol. I feel so stupid posting this and not confident with my answer. I feel like I look into it too much.

I don't believe this 12-lead shows signs associated with pulmonary embolism (PE), and the history doesn't make me think so either. In a PE, I've learned that if there is ECG changes (PE doesn't mean they'll have ECG changes):

[ ] usually the patient is tachycardic (this patient isn't tachycardic).
[ ] they'll have a pseudo RBBB (this patient has a RBBB).
[ ] ST depression and/or retrograde T-wave in V1-V4.
[ ] right ventricular strain pattern (S1Q3T3) (this patient only has an S-wave in I).
[ ] right atrial enlargement (maybe you could say the p-wave in II is p-mitral, maybe, but per Chou's book, tall t-waves in II is not specific for RAE or LAE).

When I read the history and looked at this ECG, PE didn't pop up in my mind.

NSR, RBBB+LAFB, LAE. ST Depression in I, AVL & Q waves in V1, V2, V3 w/ isoelectric ST segment. Probable Septal Stemi. Remember w/ RBBB Sgarbossa's criteria does not apply. The only st segment changes that are normal on a 12 lead w/ RBBB is minimal st depression in leads v1-v3, and this patient has st segment that is isoelectric w/ q waves. Serial 12 lead ECG's are warranted.
I'd also be concerned w/ Pulmonary Embolism, but there are not any significant indicators on this 12 lead showing Actue PE. The most important indicator for acute pe are a combination of right ventricular strain patterns including RBBB/IRBBB, S1Q3T3, RAD, and most importantly inverted T waves in the inferior/anterior leads.

It sounds like this gentleman has completed his anterior infarction and found himself in some manner of decompensated heart-failure. Prehospital treatment will be mostly supportive and focused on not making things worse for the patient. Given the large nature of his infarction you have to worry about mechanical complications of MI as well, such as mitral valve dysfunction/rupture or free-wall rupture.
I'd be a bit hesistant to break out the furosemide as most of the patients I meet with this presentation are actually a bit dehydrated to begin with, having been unwell and exhibiting poor fluid intake for several days.
I'm quite comfortable taking care of most cardiac patients, but these ones always worry me. They're not acutely sick enough to warrant pressor agents and a full-court press to combat imminent death, but they're also by no means stable as evidenced by his BP and "sick" look. Tread lightly and obtain an early cardiology consult would be my recommendation.

Oh and don't forget that he might be septic. There's no proof that his MI is actually that recent…

I think Vince is spot on. My ECG analysis was identical, but I personally wasn't smart enough to pick up on the possibility of HF secondary to recently completed infarction. I agree, though. With the minor exception that given the recent round of antibiotics, I would knock sepsis further down on my ddx. Also, for many of the reasons Andrew listed, I too think PE is unlikely (dispite the R/S trans in V1).
This is definitely a tricky case, so nice pick David! I think CPAP is key to the tx regimen. Although it can (in some articles/protocols) be contraindicated in hypotension, I think the benefit outweighs the risk here. Having said that, I would also heavily consider stacking 250cc NS boluses with a bat's ear to his lung sounds. Even though he has no compensatory tachycardia, his lack of fluid intake can't be helping his blood pressure. Besides, if we can safely bump it up even a little, a gentle touch of mainstay nitrates could help ease the heart failure symptoms.
Admittedly, I don't have a vast wealth of experience with CPAP and hypotension. A few cases personally witnessed, and numerous articles. Most say the increase in ITP causes reduced afterload, easing the heart, but also reduced preload, possibly detrimental if hovering the borders of cardiogenic shock (like our friend here). A JEMS article suggested dopamine, but with the possible dehydration, I'm not sure that's the greatest choice either. So any thoughts, anecdotes, or info here wouldn't go unappreciated ūüėČ

Would like a little more information regarding symptoms, vital signs etc, but my first thought with this patient would be that he is septic.
I would like to know lung & heart sounds, full set of obs (inc. temperature and BGL). I would like to know whether he has had any chest pain, and what this is like, a bit more about this cough (is it productive?). I would like to know his PMH and medications, and to see an old ECG if possible.
My DDx would be: ?sepsis, ?PE, ?heart failure, ???pericarditis (due to the recent ?URTI)

It's an interesting case, I think it could be either subacute anteroseptal MI or PE, despite the lack of ECG signs. The only changes suggestive of MI on the ECG are the Q-waves in V1-3, which matches the two week history but maybe not the recent worsening (when did it exactly started?). The ECG is also not really indicative of PE, only the RBBB is there. However, with dyspnoe, cough, decreased ability to excercise, hypotension, history of smoking put together I would try to rule out PE first then MI. First, vitals, then physical examination (signs of HF, DVT), thoroug history of symptoms (any king of chest pain), ABG, labs (D-dimer, necroenzymes), echocardiography, leg ultrasound, CTA. As for treatment: if he does not have left HF, then fluids (if there is right HF, cautiosly), O2, catecolamines, heparin.

I see a RBBB, left anterior hemi block, and a 1st degree block (although no one mentioned this so maybe I'm misdiagnosing, but that would be a trifasciular block). I don't agree with saying it's a PE based on the 12 lead just because of shortness of breath and RBBB. The S1Q3T3 pattern isn't present and a PE doesn't cause congestion symptoms. I'm also going with the old MI leading to heart failure diagnosis.
The location I'd assume infarcted is the septum. The AV node is damaged, evidenced by a trifasciular block. Instead of an rSR' in V1 (normal for RBBB), we have a qR. I believe this is evidence for necrotic tissue in the septal and anterior area.

I see very subtle st seg elevation of one mm in 2, and 3. I see reciprocal changes in the high lateral leads, and I see hypotension. The septum is supplied 60 % by the RCA , and 40 % by the LAD.. This would explain the right bundle branch block, right is thinner then left, as well as hypotension.. CPAP would be detrimental.. Dopamine infusion would be best, while you give ASA, during the trip to the cath lab.. Don’t forget to rule out RV infarct…

It is shown a synus rhytm with normal Pr left anterior hemyblock , q waves in v1-v4, right electric predominante and diffuse rep abnormalities Also in avl.
We see a pseudo right bundle branch block
I would point on the q waves and intra ventricolar cobduction defecar suggesting In first istance a previous Infarction of un known date and possibly a dilatative adaptation. Secondary a pulmonary ipothesis is possible.
As Medical algorithm I would do saturation echo scan of the heart , thoracic x Ray , then decide for cath lab or TC scan if pulmonary emboliam is suspected .

Ben WallerWhy do we send so many people to a cardiac arrest?I am also a Battalion Chief in Tom's system. In addition to the AHA bullets he mentioned regarding high-quality CPR, our response is designed to provide fatigue-free CPR by sending enough people so that no one does CPR for more than 2 consecutive minutes. As for science, we believe strongly in it, but we also…
2016-12-08 11:29:19

Vince DiGiulioNo, doubling the paper speed will not reveal hidden P-wavesGreat tip! It's not much of an option prehospital, but one more thing I'll do when I'm in the ED and a patient has persistent tachycardia is look at the graphic trend of the patient's heart rate. Reentrant tachycardias will show a stable horizontal line (steady rate), often with a fairly abrupt onset/offset, while sinus…
2016-12-07 06:58:16

Vince DiGiulio59 Year Old Female: Intermittent Head Pain (Conclusion)Thanks! There's a couple of reasons why V7-9 might have been negative here: 1) Not all "inferoposterior" STEMI's show ST-elevation in V7-V9. Sometimes the ST-depression we see in V2 and V3 is reciprocal to the inferior STEMI and not really caused by posterior injury. 2) You'll notice that there is only subtle ST-depression in V3…
2016-12-07 06:55:27

Cardiac Care Show - Episode 1: Mechanical CPR - ECG Medical TrainingAdvanced Airway Management – Should Paramedics Be Intubating?[…] in the Resuscitation group on Facebook and the #FOAMed community¬†on¬†Twitter. Alongside tracheal intubation, response times, and fire-based EMS, this is one of the most controversial topics in prehospital […]
2016-12-04 18:26:57